Assistant Professor, University of Virginia, Dept Neuroscience & Center for Brain Immunology & Glia (BIG)
Seminar abstract: Microglia are brain-resident immune cells with a repertoire of functions in the developing, mature and pathological brain. Despite these known roles for microglia, the extent of their interactions with the vasculature and potential regulation of vascular physiology has been insufficiently explored. Here, we document steady-state interactions between ramified CX3CR1+ myeloid cell somata and capillaries in the brain. We confirm that these myeloid cells are bona fide microglia then give a detailed spatio-temporal characterization of these capillary-associated microglia (CAMs) comparing and contrasting them with parenchymal microglia (PCMs). Molecularly, we identify microglial-specific purinergic P2RY12 receptors as a receptor regulating CAM interactions under the control of released purines from pannexin 1 channels. Furthermore, microglial elimination triggered capillary dilation, blood flow increase, and impaired vasodilative responses. Consistent with a specific role for microglia, we find that a genetic P2RY12 deficiency as well as a genetic deficiency of pannexin 1 channels is sufficient to recapitulate these vascular impairments suggesting purines released through pannexin channels play important roles in activating microglial P2RY12 receptors to regulate neurovascular structure and function. host: Oscar Vivas
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